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Characterization of resistance to prexasertib in ovarian cancer cell line OVCAR5

ABSTRACT: Characterization of resistance to prexasertib in ovarian cancer cell line OVCAR5

PROVIDER: PRJNA629799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11680544_1.fastq.gz	Fastqsanger.gz
	SRR11680544_2.fastq.gz	Fastqsanger.gz
	SRR11680545_1.fastq.gz	Fastqsanger.gz
	SRR11680545_2.fastq.gz	Fastqsanger.gz
	SRR11680546_1.fastq.gz	Fastqsanger.gz

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Characterization of resistance to prexasertib in ovarian cancer cell line OVCAR5

Project description:We developed a CHK1 inhibitor Prexasertib resistant strain of ovarian cancer cell line OVCAR5 in lab. This was used to compare transcriptome profiles to study changes in expression profiles of genes that might be involved with resistance. Total RNA was isolated from three replicate cultures of OVCAR5R (IC50 viability >3 micromolar Prexasertib) and 3 replicate cultures of parental OVCAR5 (IC50 viability=7.5nM) and then subjected to Hiseq4000 illumina RNA-seq analysis, with paired end sequencing. Data file contains CPM-TMM values after zoom normalization.

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Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (RNA-seq)

Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

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Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (ChIP-seq)

Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

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Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells

Project description:Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells

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Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells

Project description:Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells

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Effect of prexasertib on disease progression and survival in High grade serous ovarian cancer patients

Project description:The goal of this study was to compare transcription profiles of high grade serous ovarian cancer (HGSOC) patients at Day 0 and Day 15 of a single course Prexasertib treatment at 105mg/m2 intravenously over 1 hour. HGSOC patients recruited for this study were women aged 18 and older with most (79%) showing platinum resistant or refractory disease. Total RNA from patients before (Day 0, n=18) and 2 weeks after Prexasertib treatment (Day15, n=11) were prepared from frozen biopsies, and analysed using HiSeq4000 using Illumina TruSeq Stranded Total RNA Library Prep and paired-end sequencing. Data is shown as quartile normalized CPM-TMM values. Patient survival and response was monitored till end of study. Our study show that prexasertib has clinical benefit in HGSOC patients.

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A pan-cancer transcriptome analysis to identify the molecular mechanism of prexasertib resistance [microarray]

Project description:The combined influence of oncogenic drivers, genomic instability, and/or DNA damage repair deficiencies increases replication stress in cancer. Cells with high replication stress rely on the upregulation of checkpoints like those governed by CHK1 for survival. Previous studies of the CHK1 inhibitor prexasertib demonstrated activity across multiple cancer types. Therefore, we sought to (1) identify markers of prexasertib sensitivity and (2) define the molecular mechanism(s) of intrinsic and acquired resistance using preclinical models representing multiple tumor types. Our findings indicate that while cyclin E dysregulation is a driving mechanism of prexasertib response, biomarkers associated with this aberration lack sufficient predictive power to render them clinically actionable for patient selection. Transcriptome analysis of a pan-cancer cell line panel and in vivo models revealed an association between expression of E2F target genes and prexasertib sensitivity and identified innate immunity genes associated with prexasertib resistance. Functional RNAi studies supported a causal role of replication fork components as modulators of prexasertib response. Mechanisms which protect cells from oncogene-induced replication stress may safeguard tumors from such stress induced by a CHK1 inhibitor, resulting in acquired drug resistance. Furthermore, resistance to prexasertib may be shaped by innate immunity. We included microarray data here as part of the study. RNAseq data was uploaded separately.

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